Identification of bioactive compounds in Brassica oleracea var. capitata L. with enzyme-inhibitory activity against postprandial hyperglycemia

Postprandial hyperglycemia is a hallmark of diabetes, and inhibition of key carbohydrate digestion enzymes such as alpha-amylase (alpha-AMY) and alpha-glucosidase (alpha-GLU) is an effective therapeutic target. A potential unexplored source of inhibitory compounds of these enzymes is Brassica oleracea var. capitata L (BOCE). This study explored the in vitro inhibition mechanism of BOCE and studied in silico the interaction of its compounds identified and quantified by UPLC-QTOF-MS on alpha-AMY and alpha-GLU. BOCE demonstrated IC50 values of 3.08 mg/mL for alpha-AMY and 22.63 mg/mL for alpha-GLU, indicating competitive and mixed-type inhibitions, respectively. Untargeted metabolomics identified 21 compounds, primarily phenolic acids such as t-cinnamic, sinapic, and caffeoylquinic acid. In the targeted analysis, 11 compounds were quantified, mainly phenolic acids. The most impactful biosynthetic pathways identified were phenylpropanoids and brassinosteroids. In silico analysis revealed that for alpha-AMY and alpha-GLU, castasterone and 26-hydroxybrassinolide displayed the lowest binding free energies with specific hydrogen bond patterns to catalytic residues in the binding site, respectively. B. oleracea is a promising source of compounds with the ability to modulate key enzymes related to hyperglycemia. Specifically, compounds such as castasterone and 26-hydroxybrassinolide show potential against alpha-AMY and alpha-GLU inhibition, offering a novel approach to diabetes.